ArticleCancer medicine2023
TRIM55 inhibits colorectal cancer development via enhancing protein degradation of c-Myc.
Article in Cancer medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Targeting phase separation: a new strategy to disrupt the stromal-immune axis in colorectal cancer.Cell communication and signaling : CCS · 2026Review
- PLAAT2 suppresses gastric cancer progression by facilitating cMyc ubiquitination and inhibiting MEK/ERK signaling.Cell death & disease · 2026Article
- TRIM55 suppresses inflammatory response after spinal cord injury by accelerating the ubiquitination and degradation of TLR4.Journal of orthopaedic surgery and research · 2025Article
- TRIM55 restricts the progression of hepatocellular carcinoma through ubiquitin-proteasome-mediated degradation of NF90.Cell death discovery · 2024Article
- The feedback loop of EFTUD2/c-MYC impedes chemotherapeutic efficacy by enhancing EFTUD2 transcription and stabilizing c-MYC protein in colorectal cancer.Journal of experimental & clinical cancer research : CR · 2024Article
- Exploring the Mechanisms, Biomarkers, and Therapeutic Targets of TRIM Family in Gastrointestinal Cancer.Drug design, development and therapy · 2024Review
- TRIM55 inhibits colorectal cancer development via enhancing protein degradation of c-Myc.Cancer medicine · 2023Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundColorectal cancer (CRC) is one of the most common and lethal malignancies which including colon and rectum cancer. Tripartite motif containing 55 (TRIM55) is an E3 ubiquitin ligase belonging to the TRIM family. Although the aberrant TRIM55 expression has been implicated in several tumors, its functional role, and molecular mechanisms in CRC remain unknown.
methodsImmunohistochemical studies, qRT-PCR, and Western blot were performed to analyze the expression of TRIM55 in CRC patients and cell lines. TRIM55 expression and its relevance to clinical traits and prognosis were further explored in the TCGA database, and in our 87 clinical samples. Subsequently, we performed a series of functional assays to explore the effect of TRIM55 on CRC progression. Finally, the molecular mechanism of TRIM55 was investigated by immunoprecipitation and ubiquitination analyses.
resultsHere, we demonstrated that TRIM55 was markedly downregulated in CRC cell lines and tumors from CRC patients. Moreover, overexpression of TRIM55 could suppress CRC cell growth in vitro and inhibit CRC xenograft tumor development in vivo. Additionally, TRIM55 overexpression dampened CRC cell migration and invasion. Further bioinformatics analysis indicated that TRIM55 suppressed cyclin D1 and c-Myc expression. Mechanistically, co-immunoprecipitation assay revealed that TRIM55 directly interacted with c-Myc and down-regulated its protein expression level via protein ubiquitination. Intriguingly, c-Myc overexpression partially antagonized the function of TRIM55 overexpression.
conclusionsTaken together, our findings suggest that TRIM55 inhibits CRC tumor development via, at least in part, enhancing protein degradation of c-Myc. Targeting TRIM55 could provide a new therapeutic approach for CRC patients.
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